Kengo Yoda

A study of profound hypothermia by surface cooling.

Profound hypothermia below 20° C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.Résumé Ľhypothermie profonde (T° inférieure à 20° C) par réfrigération externe (immersion dans un bain ďeau glacée) sous anesthésie profonde à ľéther et ľemploi ďagents bloqueurs du système nerveux autonome ont été utilisés pour permettre la chirurgie à cœur-ouvert sans circulation extracorporelle et des arrêts circulatoires ďau-delà ďune heure.Les niveau sanguins ďéther variaient de 40.6 à 285.7 mg/dl en cours ďanesthésie. On n’a pas observé ďarythmies et les signes vitaux sont demeurés remarquablement stables. En cours ďintervention, on a relevé une hypocarbie constante, un déficit basique marqué après ľarrêt circulatoire, la correction spontanée de ľacidose métabolique et un pH près de la normale. Le taux des catécholamines s’élevait modérément après ľarrêt circulatoire, mais les niveaux étaient loin de ceux observés dans le choc. II y avait élévation marquée de ľactivité plasmatique de la rénine, mais ľangiotensine II demeurait à des niveaux négligeables durant toute la procédure. Les lactates en excès ne changeaient pas de façon significative. On a observé de ľhyperglycémie en cours ďintervention. Un taux de mortalité de 7.7 pour cent et une incidence de complications neurologiques de 5.8 pour cent ont été observés au cours des 52 derniers cas.

Clonic convulsive movements during and on emergence from sevoflurance anesthesia.

Sevoflurane is a new potent volatile anesthetic which is useful in pediatric anesthesia because of its rapid induction of and emergence from anesthesia with nonpungency and limited cardiorespiratory depression. However, clonic and tonic seizure-like movements of the extremities during induction of anesthesia with sevoflurane-nitrous oxide have been reported [1]. We previously described electrical seizures during induction of anesthesia with sevoflurane-oxygen in two pediatric patients with epilepsy [2]. In the present report, two cases are described of seizure-like activity associated with bronchospasm during induction but no bronchospasm on emergence from anesthesia with nitrous oxide-sevoflurane.

Persistent upper airway obstruction after aneurysmectomy of brachiocephalic trunk.

Tracheal compression is a well-recognized complication of aneurysm of the aortic arch and its main branches. In many cases, surgical resection of the aneurysm relieves the respiratory insufficiency and residual tracheomalacia in adults is rare. We present a case in which progressive tracheal compression caused by an aneurysm resulted in tracheomalacia and residual severe airway obstruction even after surgical repair of the aneurysm. The patient was subsequently treated with plastic repair of the trachea with a favorable result.

Comparative study on the cardio-respiratory change during prostaglandin E1-induced hypotension in the patients in the supine and prone position

Prostaglandin E1-induced hypotension (25% reduction from the preadministration level in mean arterial pressure) was applied to thirteen patients. Eight patients among them were operated in the supine position (group I) and other five in the prone position (group II). The maintenance dose of PGE1 was considerably lower in group II than in group I (0.067 μg·kg−1·min−1 vs. 0.119 μg·kg−1·min−1). In group I, there was a significant increase in CI, with a significant decrease in SVRI and PVRI during PGEI-induced hypotension. Such a high dose of PGE1 (0.119 μg·kg−1·min−1) was considered to have a direct dilating action on the systemic resistance bed as well as on the pulmonary vasculature. It was considered that the suppression of hypoxic pulmonary vasoconstriction could be a mechanism to increase venous admixture during PGE1-induced hypotension. In group II, there was no significant increase in CI, and no significant decrease in SVRI and PVRI. PGE1-induced hypotension can be safely applied to the anesthetized patients, but we should be careful to apply it to the patients in the prone position, because lower dose of PGE1 can induce severe hypotension, which is not accompanied by the increase in CI as occures in the patients in the supine position.